Evidence map›Paper›PMID 26240281›Full record

ArticleMolecular and cellular biology2015

S6 Kinase- and β-TrCP2-Dependent Degradation of p19Arf Is Required for Cell Proliferation.

Tadashi Nakagawa, Takaaki Araki, Makiko Nakagawa, Atsushi Hirao, Michiaki Unno, Keiko Nakayama

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Stress-Induced Eukaryotic Translational Regulatory Mechanisms.Journal of clinical and medical sciences · 2024
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Tadashi NakagawaDivision of Cell Proliferation, ART, Graduate School of Medicine, Tohoku University, Sendai, Japan.
Takaaki ArakiDivision of Cell Proliferation, ART, Graduate School of Medicine, Tohoku University, Sendai, Japan Department of Surgery, Graduate School of Medicine, Tohoku University, Sendai, Japan.
Makiko NakagawaDivision of Cell Proliferation, ART, Graduate School of Medicine, Tohoku University, Sendai, Japan.
Atsushi HiraoDivision of Molecular Genetics, Cancer and Stem Cell Program, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Michiaki UnnoDepartment of Surgery, Graduate School of Medicine, Tohoku University, Sendai, Japan.
Keiko NakayamaDivision of Cell Proliferation, ART, Graduate School of Medicine, Tohoku University, Sendai, Japan nakayak2@med.tohoku.ac.jp.
Tohoku University · JPKanazawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The kinase mTOR (mammalian target of rapamycin) promotes translation as well as cell survival and proliferation under nutrient-rich conditions. Whereas mTOR activates translation through ribosomal protein S6 kinase (S6K) and eukaryotic translation initiation factor 4E-binding protein (4E-BP), how it facilitates cell proliferation has remained unclear. We have now identified p19(Arf), an inhibitor of cell cycle progression, as a novel substrate of S6K that is targeted to promote cell proliferation. Serum stimulation induced activation of the mTOR-S6K axis and consequent phosphorylation of p19(Arf) at Ser(75). Phosphorylated p19(Arf) was then recognized by the F-box protein β-TrCP2 and degraded by the proteasome. Ablation of β-TrCP2 thus led to the arrest of cell proliferation as a result of the stabilization and accumulation of p19(Arf). The β-TrCP2 paralog β-TrCP1 had no effect on p19(Arf) stability, suggesting that phosphorylated p19(Arf) is a specific substrate of β-TrCP2. Mice deficient in β-TrCP2 manifested accumulation of p19(Arf) in the yolk sac and died in utero. Our results suggest that the mTOR pathway promotes cell proliferation via β-TrCP2-dependent p19(Arf) degradation under nutrient-rich conditions.

Indexed as

Cell ProliferationAnimalsbeta-Transducin Repeat-Containing ProteinsCells, CulturedCyclin-Dependent Kinase Inhibitor p19FemaleHEK293 CellsHumansMaleMiceMice, 129 StrainMice, Inbred C57BLMice, TransgenicMouse Embryonic Stem CellsPhosphorylationProtein Processing, Post-Translationalbeta-Transducin Repeat-Containing ProteinsCdkn2d protein, mouseCyclin-Dependent Kinase Inhibitor p19Fbxw1b protein, mouseRibosomal Protein S6 Kinases, 90-kDaRps6ka1 protein, mouse

Identifiers

PMID26240281
PMCPMC4573705
OpenAlexW1859240609

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.